Striated muscle in Duchenne's dystrophy is characterized by the presence of scattered foci of degenerating myofibers. Within these foci, numerous myogenic cells in various stages of regeneration represent the muscles potential for repair. In older patients (more than 5 years), regeneration becomes abnormal and eventually has no influence on the clinical progress of dystrophic degeneration. It is proposed that in early stages of the disease, only mature regenerating fibers succumb to the pathological defect, while later regenerative failure is due to a direct affect upon the myogenic stem cell. The aim of the proposed study is to analyze the nature and influence of the regenerative response in the progression of Duchenne's dystrophy. Toward this end, the population, distribution and behavior of satellite cells will be examined in both human and murine dystrophies. In addition to the structural and morphometric studies on biopsies, the dynamics of satellite cell development will be analyzed in clonal tissue culture. A myoblast-fibroblast modulation is proposed to account for the characteristic loss of regenerating stem cells and the simultaneous increase in interstitial fibrosis. This hypothesis will be examined by following the fate of labeled cells from clonal cultures that have been transplanted into normal and dystrophic hosts. A potential connective tissue-microvascular contribution to a possible ischemic etiology of Duchenne's dystrophy will be examined using fine structure and tissue culture assays.